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CB1 receptor activation in the basolateral amygdala produces antinociception in animal models of acute and tonic nociception.
Clin Exp Pharmacol Physiol. 2007 May-Jun; 34(5-6):439-49.CE

Abstract

1. Recent studies have suggested that the basolateral nucleus of the amygdala (BLA) participates in the processing of pain information, especially noxious somatic information. Cannabinoid receptors or CB1 mRNA are expressed more in the BLA than in other nuclei of the amygdala. Thus, the aim of the present study was to examine whether CB1 receptors in the BLA may be involved in modulating acute and/or tonic nociceptive processing. 2. Adult rats were exposed to intra-BLA microinjection of the cannabinoid receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl) pyrrolo [1,2,3,-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate [WIN 55,212-2 (1, 2.5, 5 or 10 microg/side)] and subjected to the tail flick and formalin tests. 3. The rats demonstrated a dose-dependent increase in latency to withdraw from a thermal noxious stimulus in the tail flick test and a decrease in formalin-induced pain behaviours. The antinociceptive effects of the CB1 receptor agonist WIN 55,212-2 (10 microg/side) in both tests were attenuated in the presence of the selective CB1 receptor antagonist, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3- carboxamide (AM251; 0.55 ng/side). Administration of the CB1 receptor antagonist AM251 (0.55, 5.5, or 55.5 ng/side) alone did not alter the nociceptive thresholds in either test. Bilateral microinjection of the selective CB2 receptor antagonist N-[(1S)-endo-1,3,3-trimethyl bicyclo [2.2.1] heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; 1 microg/side) had no effect on the antinociception produced by WIN 55,212-2, suggesting that the antinociceptive actions of WIN 55,212-2 are mediated by CB1 receptors. 4. The findings suggest the existence of a CB1-mediated inhibitory system in the BLA that, when activated, can diminish responsivity to acute and tonic noxious stimuli, but that normally has no tonic effect on the response threshold of these stimuli.

Authors+Show Affiliations

Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17439413

Citation

Hasanein, Parisa, et al. "CB1 Receptor Activation in the Basolateral Amygdala Produces Antinociception in Animal Models of Acute and Tonic Nociception." Clinical and Experimental Pharmacology & Physiology, vol. 34, no. 5-6, 2007, pp. 439-49.
Hasanein P, Parviz M, Keshavarz M, et al. CB1 receptor activation in the basolateral amygdala produces antinociception in animal models of acute and tonic nociception. Clin Exp Pharmacol Physiol. 2007;34(5-6):439-49.
Hasanein, P., Parviz, M., Keshavarz, M., & Javanmardi, K. (2007). CB1 receptor activation in the basolateral amygdala produces antinociception in animal models of acute and tonic nociception. Clinical and Experimental Pharmacology & Physiology, 34(5-6), 439-49.
Hasanein P, et al. CB1 Receptor Activation in the Basolateral Amygdala Produces Antinociception in Animal Models of Acute and Tonic Nociception. Clin Exp Pharmacol Physiol. 2007 May-Jun;34(5-6):439-49. PubMed PMID: 17439413.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CB1 receptor activation in the basolateral amygdala produces antinociception in animal models of acute and tonic nociception. AU - Hasanein,Parisa, AU - Parviz,Mohsen, AU - Keshavarz,Mansoor, AU - Javanmardi,Kazem, PY - 2007/4/19/pubmed PY - 2007/8/19/medline PY - 2007/4/19/entrez SP - 439 EP - 49 JF - Clinical and experimental pharmacology & physiology JO - Clin. Exp. Pharmacol. Physiol. VL - 34 IS - 5-6 N2 - 1. Recent studies have suggested that the basolateral nucleus of the amygdala (BLA) participates in the processing of pain information, especially noxious somatic information. Cannabinoid receptors or CB1 mRNA are expressed more in the BLA than in other nuclei of the amygdala. Thus, the aim of the present study was to examine whether CB1 receptors in the BLA may be involved in modulating acute and/or tonic nociceptive processing. 2. Adult rats were exposed to intra-BLA microinjection of the cannabinoid receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl) pyrrolo [1,2,3,-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate [WIN 55,212-2 (1, 2.5, 5 or 10 microg/side)] and subjected to the tail flick and formalin tests. 3. The rats demonstrated a dose-dependent increase in latency to withdraw from a thermal noxious stimulus in the tail flick test and a decrease in formalin-induced pain behaviours. The antinociceptive effects of the CB1 receptor agonist WIN 55,212-2 (10 microg/side) in both tests were attenuated in the presence of the selective CB1 receptor antagonist, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3- carboxamide (AM251; 0.55 ng/side). Administration of the CB1 receptor antagonist AM251 (0.55, 5.5, or 55.5 ng/side) alone did not alter the nociceptive thresholds in either test. Bilateral microinjection of the selective CB2 receptor antagonist N-[(1S)-endo-1,3,3-trimethyl bicyclo [2.2.1] heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; 1 microg/side) had no effect on the antinociception produced by WIN 55,212-2, suggesting that the antinociceptive actions of WIN 55,212-2 are mediated by CB1 receptors. 4. The findings suggest the existence of a CB1-mediated inhibitory system in the BLA that, when activated, can diminish responsivity to acute and tonic noxious stimuli, but that normally has no tonic effect on the response threshold of these stimuli. SN - 0305-1870 UR - https://www.unboundmedicine.com/medline/citation/17439413/CB1_receptor_activation_in_the_basolateral_amygdala_produces_antinociception_in_animal_models_of_acute_and_tonic_nociception_ L2 - https://doi.org/10.1111/j.1440-1681.2007.04592.x DB - PRIME DP - Unbound Medicine ER -